摘要:

The authors investigated the effects of nitrous oxide (N20), ganglionic blockade, and combined infusion of epinephrine and norepinephrine (0.1 μg·kg−1·min−1each) on neurologic outcome and brain histopathology in a model of incomplete cerebral ischemia in the rat. Thirty-eight Sprague-Dawley rats were assigned to one of four groups: group 1 (n = 10) received 70% N2O in O2; group 2 (n = 12) received 70% N2O in O2)plus ganglionic blockade; and group 3 (n = 10) received 70% N2O in O2, plus ganglionic blockade and catecholamine infusion. In groups 1–3, ischemia was produced by right carotid occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Group 4 (n = 6) received 70% N2O in O2and hemorrhagic hypotension without carotid occlusion for 30 min. At the end of ischemic and nonischemic hypotension, the carotid artery was unclamped and the blood slowly reinfused. Neurologic outcome was evaluated for a 5-day period with a graded deficit score (0 = normal to 39 = stroke-related death). Brain histopathology was evaluated in coronal section at the level of the caudate nucleus according to a 6-point scale, from 0 = normal to 5 = total hemispheric infarction. Arterial blood gases,pH, and body temperature were kept constant in all groups. Compared to N2O alone (group 1), treatment with ganglionic blockade (group 2) decreased plasma catecholamines by 75% and significantly improved neurologic outcome from incomplete cerebral ischemia (P< 0.05). Administration of exogenous epinephrine and norepinephrine in the presence of N2O and ganglionic blockade (group 3) worsened neurologic outcome compared to group 2 (P< 0.05). Brain histopathology in rats surviving the 5-day examination period showed an entire range of brain tissue damage in the ischemic hemisphere. However, neurologic deficit did not predict histopathologic neuronal injury. No neurologic deficit or histopathologic damage was seen in rats treated with nonischemic hemorrhagic hypotension (group 4). The improvement of neurologic outcome after ganglionic blockade suggests direct involvement of the sympathetic nervous system in the modulation of ischemic brain damage.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

This study examinedin vitromyocardial depression by 50% N2O. Maximal isometric contractions of guinea pig right ventricular papillary muscles were studied in Tyrode's superfusate at 37° C within a gas-tight chamber. Superfusate (pH at 7.45) and chamber were equilibrated with 95% O2/5% CO2. After control measurements in 95% O2, muscles were studied with 50% N2and 50% N2O (45% O2/5% CO2) in random order with an intervening and final recovery in oxygen. Muscles were field stimulated after rest and at 0.1–3 Hz. At 37° C, muscle performance deteriorated over time with exposure to reduced oxygen; therefore, identical experiments were performed at 30° C in which no systematic deterioration occurred. Peak tension and maximum rate of tension development (dT/dtmax) were compared for each stimulation rate. At both temperatures, N2O caused a 10–15% depression of contractility as compared to that observed with nitrogen. In a second protocol, muscles were studied at 37° C in 26 mM K+Tyrode's solution with 0.10 μM isoproterenol to study enhanced contractions mediated by slow (Ca2+-channel-dependent) action potentials. Rested-state double stimulations were used (stimulus interval, 250–600 ms) resulting in a first rested-state contraction followed by a second contraction (C2) with rapid initial tension development. The muscles were exposed to nitrogen and N2O as in the force-frequency experiments and did not deteriorate over time. In this setting, N2O also caused a 10–15% depression of C2 contractility as compared with nitrogen. Another set of muscles was studied in 95% O2to which 0.5% halothane or 1% isoflurane was added before exposure to nitrogen and N2O. The combined depressant action of N2O with either halothane or isoflurane did not differ from that predicted by the simple addition of independent effects; there was no evidence of synergism. Furthermore, N2O (50%) alone depressed dT/dtmaxin a manner similar to that of 0.5% halothane and different from that of 1.0% isoflurane. Experiments conducted in iso-osmolar 40 mM Na+Tyrode's solution, in which activator Ca2+arose from the sarcoplasmic reticulum Ca2+, also showed greater depression by N2O than nitrogen. N2O (50%) is a myocardial depressant independent of concurrent hypoxic effects with a pattern and magnitude of contractile depression similar to that of 0.5% halothane.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Using the 2-[l4C]deoxyglucose method, the effects of analgesic doses of epidural bupivacaine (300 μg) on local spinal cord glucose utilization (SP-LGU) of the cervical, thoracic, and lumbar regions and local cerebral glucose utilization (BR-LGU) in 38 brain structures were examined in conscious rats. In addition, the effects of intramuscular bupivacaine (300 μg) and the spinal cord transection (T2) were examined to determine whether the induced metabolic changes, if any, are related to the drug's systemic effect and/or deafferentation. Lumbar epidural bupivacaine sufficient to produce analgesia decreased SP-LGU in the thoracic (18–28%) and lumbar (21–29%) spinal cord but not in the cervical cord. Epidural bupivacaine decreased BR-LGU (15–26%) in 35 of 38 structures examined. With intramuscular bupivacaine, SP-LGU remained unchanged in almost all regions, while BR-LGU was significantly decreased (11–23%) in 23 structures. Plasma concentrations of bupivacaine in the epidural and intramuscular groups were comparable. With spinal cord transection alone, SP-LGU significantly decreased with varying degrees depending on the structure examined, but BR-LGU did not decrease in 36 of 38 structures examined. These results indicate that analgesic doses of epidural bupivacaine decrease SP-LGU, probably reflecting decreased neuronal activity of the spinal cord, and that reduced BR-LGU by epidural bupivacaine is most likely due to the drug's systemic effect rather than deafferentation.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

To study the effect of oncotic pressure on brain water content during cardiopulmonary bypass (CPB), 14 anesthetized New Zealand White rabbits underwent 60 min of nonpulsatile CPB at normothermia. Animals were grouped according to the composition of the circuit priming fluid. Group 1 animals (n = 7) received a priming fluid (6.5% hydroxyethyl starch in 0.72 N NaCl; 323 ± 13 mOsm/ kg [mean ± SD]) that maintained normal colloid oncotic pressure (COP) during CPB (19.0 ± 1.5 mmHg). Group 2 animals (n = 7) received a priming fluid (0.9 N NaCl; 324 ± 23 mOsm/kg) that led to a hypooncotic state (COP = 6.2 ± 1.2 mmHg). Blood chemistries and hemodynamics were recorded every 15 min during CPB. Animals were given additional priming fluid and sodium bicarbonate during CPB to maintain a circuit flow of 85 ml·kg−1·min−1and arterialpH greater than 7.35. There were no significant differences between groups 1 and 2 with respect to temperature, central venous pressure, mean arterial pressure, PaO2, PaCO2on plasma sodium concentration, or osmolality at any time during CPB, although osmolality increased in both groups. After 60 min of bypass, animals were killed and organ water contents were determined by wet/dry weight ratios. A separate group of nine similarly prepared and anesthetized animals that did not undergo cannulation or CPB also underwent measurement of plasma chemistries and tissue water contents and served as nonbypass controls (group 3). Brain and kidney water contents were unaffected by oncotic pressure, whereas duodenum and skeletal muscle had significantly greater water content (P= 0.003 andP= 0.008, respectively) after hypooncotic CPB. To maintain flow andpH, group 2 (hypooncotic) animals required an average of 313 ± 82 ml additional fluid and 14 ± 7 mEq bicarbonate, whereas group 1 (isooncotic) animals required only 21 ± 27 ml additional fluid (P= 0.0001) and 3 ± 4 mEq bicarbonate (P= 0.0025). All tissue water contents were identical between the control (group 3) and group 1 animals. These results indicate that the mechanisms that maintain brain fluid balance remain intact during nonpulsatile hypooncotic CPB. Fluid and bicarbonate requirements, and edema formation in other tissue beds can be minimized by maintenance of normal oncotic pressure during CPB.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effects of halothane or cooling on Ca2+-activated tensions and on the uptake and release of Ca2+by the sarcoplasmic reticulum were investigated in chemically skinned fibers of the extensor digitorum longus muscle of adult rabbits. At 22° C, halothane (>0.46 mM) induced Ca2+release from the SR of Ca2+-loaded skinned fibers that resulted in transient tensions. Higher concentrations of halothane (>4.65 mM) reduced the steady-state accumulation of Ca2+in the SR at 22° C. Cooling (to <10° C) elicited transient contractures (cooling-induced contractures [CC]) in Ca2+-Ioaded skinned fibers, despite the fact that the tensions elicited by adding Ca2+to the bath were depressed at these low temperatures. The skinned fibers did not develop CCs at 12–16° C. Halothane cooling contractures could be elicited at these temperatures by exposing the fibers to halothane concentrations that failed to elicit Ca2+release at 22° C. The halothane cooling contractures were blocked by procaine but not by lidocaine. It was concluded that these contractures resulted from a synergistic interaction between halothane and cooling that stimulates Ca2+release from, and reduces Ca2+uptake by, the sarcoplasmic reticulum.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Right ventricular (RV) dysfunction may occur due to increased RV afterload and, hence, might also contribute to the decrease in cardiac output following institution of PEEP in patients with adult respiratory distress syndrome (ARDS). To test this hypothesis, the authors examined the influence of PEEP on local and global RV function in 12 anesthetized dogs with experimental ARDS (eARDS) induced by pulmonary microembolization with glass beads and oleic acid. Local RV function was analyzed in the RV inflow tract (RVIT) and RV outflow tract (RVOT) by assessing both diastolic segment length, systolic segment shortening, and segment work (sonomicrometry). Global RV contractility was quantified by measuring maximum rate of pressure rise (dRVP/dtmax) and maximum velocity of contractile element shortening (Vmax). In eARDS, despite a fivefold increase in pulmonary vascular resistance, there was no change in cardiac index (CI), global RV contractility, RVIT and RVOT work, and RVIT shortening, whereas RVOT shortening decreased from 12.4 to 7.4% (P< 0.01). Diastolic segment length increased in RVIT (P< 0.05) but not in RVOT. PEEP of 10 cmH2O did not alter global RV contractility, RVIT and RVOT shortening, and RVIT work but reduced RVOT work (-35%;P< 0.01) and CI (-11%;P< 0.001). Cardiac index further decreased during PEEP of 20 cmH2O (-38%;P< 0.001), while global RV contractility remained intact despite decreased RVIT and RVOT shortening (-32% and −69%;P< 0.05) and work (-26% and −59%;P< 0.01) in the presence of reduced fiber preload in both regions. From these findings, it was concluded that 1) the decreased CI during mechanical ventilation with PEEP at constant right ventricular end-diastolic pressure (RVEDP) is not caused by depressed global RV contractility in dogs with eARDS and a normal myocardium prior to insult. Decreased diastolic segment length and segment shortening during PEEP suggest that 2) PEEP reduces stroke volume by the Starling mechanism rather than by ischemia of the RV free wall. Finally, regionally incongruent changes of fiber preload indicate that 3) local differences in RV wall compliance are likely to occur subsequent to eARDS and PEEP.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The authors investigated the effects of halothane (HAL) and isoflurane (ISO) on cardiac depression produced by global hypoxia and the recovery of function following reoxygenation in isolated guinea pig hearts perfused with Krebs' solution at constant pressure. Isovolumetric left ventricular systolic (LVSP) and end-diastolic pressures (LVEDP) were measured by placing a saline filled, latex balloon into the left ventricle. Bipolar electrodes were placed in the right atrium and right ventricle for measurement of heart rate (HR), atrioventricular conduction time (AVCT), and determination of the incidence and severity of dysrhythmias occurring during hypoxia and reoxygenation. Hearts were divided into three groups: control (n = 20), halothane (n = 12), and isoflurane (n = 13). All hearts were exposed in sequence to oxygenated perfusate (Po2530 mmHg), moderately hypoxic perfusate (PO2, 91 mmHg) for 30 min, and then to oxygenated perfusate for 40 min. Halothane (1%, 0.4 mM) or isoflurane (1.5%, 0.5 mM) were administered 10 min before hypoxia, during hypoxia, and during the first 10 min of reoxygenation. Exposure to halothane and isoflurane before hypoxia produced a 14 and 11% decrease in heart rate, a 32 and 23% increase in AVCT, and a 47 and 28% decrease in LVSP (all P ≤ 0.001) for halothane and isoflurane, respectively, and no significant change in LVEDP. During hypoxia, HR decreased and AVCT increased similarly in both groups. Left ventricular systolic pressure (LVSP) decreased sharply with a narrowing of the prehypoxic differences among the groups. In the control and isoflurane groups, LVEDP increased during hypoxia but remained unchanged in the halothane group. After 40 min of reoxygenation, LVEDP in the control group (11 ± 3 mmHg) was significantly higher than in the halothane group (0.5 ± 1.0 mmHg) but not significantly different from the isoflurane group (5.5 ± 3.0 mmHg). Halothane reduced the incidence of ventricular tachycardia from 80 to 42% and of ventricular fibrillation from 70 to 17% during the 30-min period of hypoxia and during the first 30 min of reoxygenation, respectively, and produced a threefold increase in the average time the hearts were in sinus rhythm. The results indicate that halothane protects the isolated heart against hypoxic damage as assessed by improved recovery of LVSP, reduced LVEDP, and reduced incidence and duration of dysrhythmias during hypoxia and reoxygenation. The mechanism of protection by halothane could be related to reduced cardiac work before and after hypoxia or possibly to other direct protective myocardial cellular effects.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The mechanism of action of inhalational anesthetics is unknown, but neuronal membrane alteration is a favored hypothesis. Since phospholipid methylation and translocation play a key role in the transmission of biologic signals across cell membranes, we examined the effect of two commonly used halogenated anesthetics, halothane and isoflurane, on phospholipid methylation in rat brain synaptosomes. Using S-adenosyi-L-[3H-methyl]methionine as a donor, we found a two-fold increase in3H-methyl incorporation into phospholipids in synaptosomes taken from rats exposed to concentrations that just abolish pain response, but not in rats exposed to higher or lower concentrations. Methylation was not increased in rats newly recovered from anesthesia. Halothane added to synaptosomes taken from rats not previously exposed to anesthetics stimulated3H-methyl incorporation over a wide range of concentrations. Enhancement of phospholipid methylation by halothane and isoflurane may effect an alteration of neural signal transduction that results in the anesthetic state.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Adenosine has sedative properties, and adenosine-receptor agonists have been found to reduce anesthetic requirements in rodents. This study determined whether adenosine, in hypotensive doses, reduces anesthetic requirements in halothane-anesthetized dogs. In seven animals, minimum alveolar concentration (MAC) for halothane was determined by a tail-clamp technique at three time points: after 2 h of halothane anesthesia, during adenosine-induced hypotension (mean arterial pressure: 55 mmHg), and 1 h after adenosine was discontinued. In other dogs, the effects of aminophylline, dipyridamole, or the specific adenosine-receptor antagonist 8-phenyl-theophylline (8-PT) on the halothane-adenosine interaction were studied. Adenosine significantly reduced halothane MAC, by 49%, from 0.76 ± 0.05 to 0.39 ± 0.05 vol% (mean ± SEM). This effect was blocked by the concurrent administration of aminophylline (n = 5,P< 0.05) or 8-PT (n = 4 of 4). When dipyridamole, which increases the plasma concentrations of endogenous adenosine, was administered alone, halothane MAC was reduced from 0.79 ± 0.03 to 0.67 ± 0.05 vol% (n = 5,P= 0.09). We conclude that exogenous adenosine substantially reduces halothane MAC in dogs and that this effect is blocked by the concurrent administration of the adenosine-receptor antagonists aminophylline or 8-PT. Relatively small alterations of endogenous adenosine concentrations, however, do not substantially reduce halothane MAC.

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1990

数据来源: OVID